Abstract

Hemodynamic monitoring is used to identify deviations from hemodynamic goals and to assess responses to therapy. To accomplish these goals one must understand how the circulation is regulated. In this review I begin with an historical review of the work of Arthur Guyton and his conceptual understanding of the circulation and then present an approach by which Guyton's concepts can be applied at the bedside. Guyton argued that cardiac output and central venous pressure are determined by the interaction of two functions: cardiac function, which is determined by cardiac performance; and a return function, which is determined by the return of blood to the heart. This means that changes in cardiac output are dependent upon changes of one of these two functions or of both. I start with an approach based on the approximation that blood pressure is determined by the product of cardiac output and systemic vascular resistance and that cardiac output is determined by cardiac function and venous return. A fall in blood pressure with no change in or a rise in cardiac output indicates that a decrease in vascular resistance is the dominant factor. If the fall in blood pressure is due to a fall in cardiac output then the role of a change in the return function and cardiac function can be separated by the patterns of changes in central venous pressure and cardiac output. Measurement of cardiac output is a central component to this approach but until recently it was not easy to obtain and was estimated from surrogates. However, there are now a number of non-invasive devices that can give measures of cardiac output and permit the use of physiological principles to more rapidly appreciate the primary pathophysiology behind hemodynamic abnormalities and to provide directed therapy.

Highlights

  • A basic premise for the management of hemodynamic instability is that a response to a therapy can only be in the range of the physiologically possible

  • Before Guyton, control of cardiac output was primarily considered in terms of heart rate, stroke volume, and function of the heart [1] and little thought was given to the importance of how blood gets back to the heart [2]

  • Guyton credited Ernest Starling for appreciating that output from the heart is dependent upon the return of venous blood and that venous return is dependent upon the pressure upstream to the heart in the systemic circulation, which Starling called mean systemic pressure

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Summary

Introduction

A basic premise for the management of hemodynamic instability is that a response to a therapy can only be in the range of the physiologically possible. If the venous return curve intersects the ascending part of the cardiac function curve, CVP falls during inspiration relative to atmospheric pressure (Figure 5) and output from the right heart transiently increases because the heart is effectively lowered relative to the venous reservoir, which allows more blood to come back to the heart. Patients who do not have an inspiratory fall in CVP may or may not have a fall in cardiac output depending on how much the cardiac function curve is shifted to the right of the venous return curve with the increase in pleural pressure We tested these predictions in patients who had spontaneous inspiratory efforts and in whom positive endexpiratory pressure was going to be increased [28]. The variations during single breaths that we used for volume responsiveness are too short for there to be reflex adjustments

Conclusion
Magder S
Rothe CF
14. Brengelmann GL
20. Green JF
Findings
27. Magder S
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